ReviewAging cell2014
The replicometer is broken: telomeres activate cellular senescence in response to genotoxic stresses.
Review in Aging cell, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
30 citing papers in PubMed.
- PQQ Modulates Cell Cycle and DNA Replication Programs to Alleviate Replicative Senescence in Human Umbilical Cord Mesenchymal Stromal Cells.Stem cell reviews and reports · 2026Article
- The Role of Cellular Senescence and SASP in the Pathogenesis of Atherosclerosis and the Therapeutic Potential of Senolytic Strategies in Cardiovascular Diseases.Biomedicines · 2026Review
- Senescent CD8 T Effector Memory Cells are Functionally Impaired, Enriched in Aging and Disease, and a Barrier to Immunotherapy.bioRxiv : the preprint server for biology · 2025Article
- The complex interplay between aging and cancer.Nature aging · 2025Review
- Telomeric DNA breaks in human induced pluripotent stem cells trigger ATR-mediated arrest and telomerase-independent telomere damage repair.Journal of molecular cell biology · 2024Article
- Telomerase inhibitors TMPyP4 and thymoquinone decreased cell proliferation and induced cell death in the non-small cell lung cancer cell line LC-HK2, modifying the pattern of focal adhesion.Brazilian journal of medical and biological research = Revista brasileira de pesquisas medicas e biologica · 2023Article
- Article
- Do the telomere ends justify the physical means?Journal of the American Geriatrics Society · 2021Article
- Telomeres and replicative cellular aging of the human placenta and chorioamniotic membranes.Scientific reports · 2021Article
- Peripheral blood leukocyte telomere length is associated with survival of sepsis patients.The European respiratory journal · 2020Observational
- The many types of heterogeneity in replicative senescence.Yeast (Chichester, England) · 2019Review
- Back to the future: The intimate and evolving connection between telomere-related factors and genotoxic stress.The Journal of biological chemistry · 2019Review
- Adaptation to DNA damage checkpoint in senescent telomerase-negative cells promotes genome instability.Genes & development · 2018Article
- Targeting the DNA Damage Response in OSCC with TP53 Mutations.Journal of dental research · 2018Review
- Review
- A regulatory loop connecting WNT signaling and telomere capping: possible therapeutic implications for dyskeratosis congenita.Annals of the New York Academy of Sciences · 2018Review
- Article
- The protein subunit of telomerase displays patterns of dynamic evolution and conservation across different metazoan taxa.BMC evolutionary biology · 2017Article
- Stem cells in degenerative orthopaedic pathologies: effects of aging on therapeutic potential.Knee surgery, sports traumatology, arthroscopy : official journal of the ESSKA · 2017Review
- Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors.
Funding
Abstract
Telomeres, the ends of our linear chromosomes, can function as 'replicometers', capable of counting cell division cycles as they progressively erode with every round of DNA replication. Once they are critically short, telomeres become dysfunctional and consequently activate a proliferative arrest called replicative senescence. For many years, telomeres were thought to be autonomous structures, largely isolated from cell intrinsic and extrinsic signals, whose function is to prevent limitless cellular proliferation, a characteristic of most cancer cells. It is becoming increasingly evident, however, that telomeres not only count cell divisions, but also function as sensors of genotoxic stresses to stop cell cycle progression prematurely and long before cells would have entered replicative senescence. This stable growth arrest, triggered by dysfunctional telomeres that are not necessarily critically short, likely evolved as a tumor-suppressing mechanism as it prevents proliferation of cells that are at risk for acquiring potentially hazardous and transforming mutations both in vitro and in vivo. Here, we review studies supporting the concept that telomeres are important cellular structures whose function not only is to count cell divisions, but also to act as molecular switches that can rapidly stop cell cycle progression permanently in response to a variety of stresses, including oncogenic signals.
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What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.